D i ffe re n t i a l D i a g n o s i s

o f Tem p o ro m a n d i b u l a r
D i s o rde r s an d O t h e r
O ro f a c i a l Pa i n
D i s o rde r s
a, b
Jeffrey P. Okeson, DMD *, Reny de Leeuw, DDS, PhD

KEYWORDS
 Temporomandibular disorders
 Temporomandibular joint disorders  Neuropathic pain
 Migraine  Tension type headache

The focus of this article is on the differential diagnosis of pain disorders that typically
fall outside the realm of dental diseases. There are a great variety of such conditions—
too many to review here. Therefore, this article discusses the differential diagnosis of
a few of the more common orofacial pain conditions the dentist may face in a practice.
These conditions are divided into two sections: temporomandibular disorders (TMD)
and other common orofacial pain disorders. The first section reviews common TMD
that are the responsibility of the dentist to identify and manage. The second section
reviews some common orofacial pain disorders that the dentist needs to recognize
but for which the dentist may not be the primary care provider.

TMD

TMD is a collective term that includes a number of clinical complaints involving the
muscles of mastication, the temporomandibular joint (TMJ), or associated orofacial
structures.1 TMD are a major cause of nondental pain in the orofacial region and
are considered a subclassification of musculoskeletal disorders. In many TMD
patients the most common complaint originates from the muscles of mastication
rather than from the TMJ. Therefore, the terms TMJ dysfunction or TMJ disorder
are inappropriate for many complaints arising from the masticatory structures. It is

a
Department of Oral Health Science, Division of Orofacial Pain, D-142, College of Dentistry,
University of Kentucky, 800 Rose Street, Lexington, KY 40536-0297, USA
b
Division of Orofacial Pain, D-530, College of Dentistry, University of Kentucky, 800 Rose
Street, Lexington, KY 40536-0297, USA
* Corresponding author.
E-mail address: [email protected]

Dent Clin N Am 55 (2011) 105–120

doi:10.1016/j.cden.2010.08.007 dental.theclinics.com
0011-8532/11/$ – see front matter Ó 2011 Elsevier Inc. All rights reserved.
106 Okeson & de Leeuw

for this reason that the American Dental Association adopted the term “temporoman-
dibular disorder.”2
Signs and symptoms associated with TMD are a common source of chronic pain
complaints in the head and orofacial structures. These complaints can be associated
with some generalized musculoskeletal problems and even somatization, anxiety, and
depression. The primary signs and symptoms associated with TMD originate from the
masticatory structures and, therefore, are associated with jaw function. Patients often
report pain in the preauricular areas, face, or temples. Reports of pain during mouth
opening or chewing are common. Some individuals may even report difficulty
speaking or singing. TMJ sounds are also frequent complaints and maybe described
as clicking, popping, grating, or crepitus. In many instances, the joint sounds are not
accompanied by pain or dysfunction, and are merely a nuisance to the patient.
However, on occasion, joint sounds may be associated with locking of the jaw during
opening or closing, or with pain. Patients may even report a sudden change in their
bite coincident with the onset of the painful condition.
It is important to appreciate that pain associated with most TMD is increased with
jaw function. Because this is a condition of the musculoskeletal structures, function of
these structures generally increases the pain. When a patient’s pain complaint is not
influenced by jaw function, other sources of (orofacial) pain should be suspected.
TMD can be subdivided into two broad categories related to their primary source of
pain and dysfunction: masticatory muscle disorders and intracapsular (TMJ) disor-
ders. A description of the most common disorders in each category is reviewed below.
A more complete review of TMD can be found elsewhere.3

Masticatory Muscle Disorders

Definition
Functional disorders of masticatory muscles are probably the most common TMD
complaint of patients seeking treatment in the dental office. With regard to pain, they
are second only to odontalgia (ie, tooth or periodontal pain) in terms of frequency.
They are generally grouped in a large category known as masticatory muscle disorders.

Clinical features
The two major symptoms of functional TMD problems are pain and dysfunction.
Certainly the most common complaint of patients with masticatory muscle disorders
is muscle pain, which may range from slight tenderness to extreme discomfort. Pain
felt in muscle tissue is called myalgia. The pain is commonly described in terms
such as dull, achy, or tender. The symptoms are often associated with a feeling of
muscle fatigue and tightness. Patients will usually describe the location of the pain
as broad or diffuse, and the pain is often bilateral. This complaint is quite different
than the specific location reported in intracapsular disorders.
The severity of muscle pain is generally directly related to the amount of functional
activity. Therefore, patients often report that the pain affects their ability to open their
mouth, chew, and speak. If the patient does not report an increase in pain associated
with jaw function, the disorder is not likely related to a masticatory muscle problem
and other diagnoses should be considered.
The clinician should appreciate that not all muscle pain is the same.3 Some patients
suffer with relatively simple overuse muscle pain called “local muscle soreness.” Clin-
ically, the local muscle soreness manifests as tenderness or pain on palpation. Other
patients may experience a more regional muscle condition such as myofascial pain.
Clinically, myofascial pain is characterized by the presence of localized, firm, hyper-
sensitive bands of muscle tissue called trigger points.4 These areas create a source
 Temporomandibular Disorders 107

of deep pain input that can lead to central excitatory effects resulting in pain referral.
This condition manifests as pain on palpation with referral of pain in the surrounding or
remote tissues. Sometimes these remote tissues can be teeth, and the primary
complaint that the patient may have is tooth pain. It is important that the dentist real-
izes that the site of pain is not always the same as the source of the pain. In this hypo-
thetical case of myofascial pain, there is nothing wrong with the teeth (the site of the
pain); however, it would be easy for the dentist to miss the correct diagnosis if the
muscles of mastication (the source of the pain) were not included in the diagnostic
work-up. It is also important to realize that myofascial pain originating from cervical
muscles may refer pain into the orofacial region. Treating the site of pain in these
instances would not result in improvement of the symptoms.
Dysfunction is a common clinical symptom associated with masticatory muscle
disorders. Clinically, this may be seen as a decrease in the range of mandibular move-
ment. When muscle tissues have been compromised by overuse, any contraction or
stretching increases the pain.5 Therefore, to maintain comfort, the patient restricts
movement within a range that does not increase pain. The restriction may be at any
degree of opening depending on where discomfort is felt. The restriction may also
be partly due to contraction of the antagonistic muscles, a phenomenon that is called
protective cocontraction. In many myalgic disorders the patient is able to slowly open
wider but this increases the pain.
Acute malocclusion is another condition that is often associated with masticatory
muscle pain. Acute malocclusion refers to any sudden change in the occlusal position
that has been created by a disorder. An acute malocclusion may result from a sudden
change in the resting length of a muscle that controls jaw position. When this occurs the
patient describes a change in the occlusal contacts of the teeth. The mandibular posi-
tion and resultant alteration in occlusal relationships depend on the muscles involved.
For example, the malocclusion associated with slight functional shortening of the infe-
rior lateral pterygoid is clinically evident as disclusion of the posterior teeth on the ipsi-
lateral side and premature contact of the anterior teeth (especially the canines) on the
contralateral side. With functional shortening of the elevator muscles (clinically a less
detectable acute malocclusion), the patient will generally complain of a sensation of
heavier tooth contact on the ipsilateral side. It is important to realize that an acute
malocclusion is the result of the muscle disorder and not the cause. Therefore, treat-
ment should never be directed toward correcting the malocclusion by means of
occlusal adjustments. Rather, it should be aimed at eliminating the muscle disorder.
When the muscle disorder is resolved, the occlusal condition will return to normal.

Etiologic considerations
Myalgia can arise from a number of different causes. The most common cause is an
increased level of muscle use. Although the exact origin of this type of muscle pain is
debated, some investigators suggest it is related to vasoconstriction of the relevant
nutrient arteries and the accumulation of metabolic waste products in the muscle
tissues.5 Within the ischemic area of the muscle certain algogenic substances (eg,
bradykinins, prostaglandins) are released, causing muscle pain.
Increased muscle use maybe the result of activities that are outside the normal func-
tional activities of chewing, swallowing, and speaking. Such activities are considered
parafunctional and these activities are more likely to compromise the muscle tissues
and create pain. Activities such as daytime clenching of the teeth or sleep-related
bruxing are common parafunctions that may lead to muscle pain.6 In addition to
clenching and bruxing, habits such as chewing gum and biting lips, cheeks, and finger
108 Okeson & de Leeuw

nails are also considered to be parafunctional activities. It should be appreciated that

these activities are very common and do not lead to pain in most individuals.
A misunderstood but very important concept for the clinician to appreciate is the
fact that masticatory muscle pain is not strongly correlated with increased muscle
activity such as in spasm.7–9 In fact, studies reveal that the resting activity of the masti-
catory muscles as measured by electromyography of patients with chronic muscle
pain is no different than that of asymptomatic controls. Therefore the majority of masti-
catory muscle pain patients are not experiencing spasms.
It is now appreciated that muscle pain can be influenced and actually initiated by the
central nervous system through antidromic effects leading to neurogenic inflammation
in the peripheral structures. When these peripheral structures are muscles, this is clin-
ically felt as muscle pain. This type of muscle pain is referred to as “centrally mediated
myalgia” and can be a difficult problem to manage for the dentist since the peripheral
structures, such as teeth, jaw, and muscles are not the significant cause of the pain. In
these instances, the central mechanisms need to be addressed, which cannot be
accomplished by classic dental therapies. Owing to the involvement of central mech-
anisms, increased levels of emotional stress and other sources of deep pain may likely
influence masticatory muscle pain disorders.10
Management considerations
A detailed description of the management of each of the conditions is not the goal of this
article and, therefore, other sources should be consulted. However, because some
simple behavior modifications may reduce parafunctional use of the muscles, a few
first-tier management options are described in this section. Making the patient aware
that his or her maxillary and mandibular teeth should not be touching each other except
to speak, chew, or swallow is an important first step. In addition, for most masticatory
muscle conditions, soft diet, rest, moist heat, and (possibly) nonsteroidal anti-inflamma-
tory drugs (NSAIDS) are usually helpful. Teaching the patient to keep the teeth apart and
the mouth relaxed when the jaw is not used is very beneficial if not crucial in reducing
pain.11 If sleep-related bruxism is suspected, a stabilization appliance may be helpful.
TMJ
Definition
The signs associated with functional disorders of the TMJ are probably the most
common findings when examining a patient for masticatory dysfunction. Many of these
signs do not produce painful symptoms and, therefore, the patient may not seek treat-
ment. When present, however, they generally fall into three broad categories: derange-
ments of the condyle-disc complex, structural incompatibility of the articular surfaces,
and inflammatory joint disorders. The first two categories have been collectively
referred to as disc-interference disorders. The term disc-interference disorder was first
introduced by Welden Bell12 to describe a category of functional disorders that arises
from problems with the condyle-disc complex. Some of these problems are due to
a derangement or alteration of the attachment of the disc to the condyle; others to an
incompatibility between the articular surfaces of the condyle, disc, and fossa; still others
to the fact that relatively normal structures have been extended beyond their normal
range of movement. With time, inflammatory disorders can arise from a localized
response of the TMJ tissues to loading or trauma. These disorders are often the result
of chronic or progressive disc derangement disorders.
Clinical features
The two major symptoms of functional TMJ problems are pain and dysfunction. Joint
pain can arise from healthy joint structures that are mechanically abused during
 Temporomandibular Disorders 109

function, from impingement of tissues, or from structures that have become inflamed.
Pain originating from healthy structures or impingements is felt as sharp, sudden, and
(sometimes) intense pain that is closely associated with joint movement. When the
joint is rested, the pain resolves instantly. The patient often reports the pain as being
localized to the preauricular area. If the joint structures have become inflamed, the
pain is reported as constantly dull or throbbing, even at rest, yet accentuated by joint
movement.
Dysfunction is common with functional disorders of the TMJ. Usually it presents as
a disruption of the normal condyle-disc movement often with the production of joint
sounds. The joint sounds may be a single event of short duration known as a click.
If this is loud, it may be referred to as a pop. Crepitation is a multiple, rough, gravel-
like sound described as grating or grinding. Dysfunction of the TMJ may also present
as catching sensations when the mouth is opened. Sometimes the jaw can actually
lock. Dysfunction of the TMJ is always directly related to jaw movement.
A single click during opening of the mouth is often associated with an anterior dis-
placed disc that is returned to a more normal position during the opening movement.
This condition is referred to as a “disc displacement with reduction.”3 Often when the
patient closes the mouth a second click is felt which represents the re-displacement of
the disc to the anterior displaced position (Fig. 1). This single opening click associated
with disc displacement with reduction should be fairly repeatable. When the patient
reports a single, loud, popping or cracking sound that cannot be easily repeated, the
clinician should think about the possibility of an adherence.13 An adherence can occur
as a result of prolonged static loading of the joint. In such a case, the lubrication is
squeezed out of the contacting joint surfaces and this causes the surfaces stick
together. On opening, this union can be disrupted and normal mouth opening resumes.
For some patients the disc displacement progresses and the disc may not be able to
return to its normal relationship with the condyle during opening. This condition is
referred to as a “disc displacement without reduction.”3 When this occurs, the patient
often cannot open fully because the disc is blocking the translation of the condyle. For
this reason the condition is often referred to as a “closed lock” (Fig. 2). Additional clin-
ical characteristics include a deflection to the ipsilateral side on opening and protru-
sion, and restriction of movement to the contralateral side due to the limited ability
of the condyle to translate.
Crepitation is usually related to roughness of the articular surfaces because of
remodeling or osteoarthritis. Typically this is found in patients who have experienced
a disc displacement without reduction or in whom radiographically notable bony
changes are present. It can also be a sign of perforation of the disc or the retrodiscal
tissues. If crepitation is the only symptom or sign a patient presents with, treatment is
not usually indicated. Likewise, if the patient presents with a painless clicking TMJ that
does not affect the quality of life, treatment is not indicated. However, the patient
should be reassured and educated with regard to the origin of the sounds and, if indi-
cated, instructed to avoid parafunctional activities.

Etiologic considerations
The cause of intracapsular disorders of the TMJ is most commonly related to
trauma.14–16 This trauma may manifest itself as either macrotrauma or microtrauma.
In cases of macrotrauma a single blow to the mandible can lead to a disruption of
the normal biomechanical functions of TMJ. The traumatic event typically injures joint
structures—elongating ligaments or damaging articular surfaces. Once ligaments
have been elongated their biomechanical function is changed—often creating insta-
bility of the joint. This could eventually lead to disc displacement. Instability and
110 Okeson & de Leeuw

Fig. 1. (A) Normal condyle-disc relationship. (B) Disc displacement. (C) The movement of the
condyle with a disc displacement. Note the clicking between 3 and 4, and again between 8
and 1. (Adapted from Okeson JP. Management of temporomandibular disorder and occlu-
sion. 6th edition. St Louis (MO): CV Mosby; 2008. p. 181; with permission.)

disc displacement may both cause abnormal or unfavorable loading in the TMJ, and
this may lead to osteoarthritic changes.17
Microtrauma, a small amount of loading force repeated over a long period of time,
may lead to changes in joint structures. When the teeth are brought into heavy contact
and the joint structures are loaded, there is a momentary reduction of blood flow in the
small capillaries that supply the joint structures, resulting in hypoxia (a reduced supply
of oxygen). Under circumstances of hypoxia, the metabolism of the local cell popula-
tions may alter. The byproducts of the altered metabolism may form free radicals when
oxygen becomes available again, once the load on the tissues is reduced and the
 Temporomandibular Disorders 111

Fig. 2. The movement of the condyle with a disc displacement without reduction. Note the
disc is constantly maintained in the dislocated position (a closed lock). (Adapted from Oke-
son JP. Management of temporomandibular disorder and occlusion. 6th edition. St Louis
(MO): CV Mosby; 2008. p. 185; with permission.)

capillaries are reperfused. Free radicals may also be generated by direct mechanical
trauma and tissue damage. Free radicals are very unstable molecules with a strong
affinity for electrons. If these electrons are taken from adjacent healthy tissues, the
integrity of these tissues can be compromised. This process is known as
a “hypoxia-reperfusion injury.”13,18 The subtle changes that may occur could consist
of a decrease in the lubrication quality of the synovial fluid creating more friction during
joint movement. It may also affect the articular surfaces of the joint creating a softening
of this tissue called “chondromalacia.” The compromised lubrication and softening of
articular surfaces can cause the disc to displace from its normal position between the
condyle and fossa.
Once the disc is displaced, joint loading can occur on nonarticular surfaces such as
the retrodiscal tissue behind the disc. Because these tissues are highly vascularized
and well innervated, compression often leads to pain. With further loading these
tissues can breakdown allowing the condyle to directly load the articular fossa.
Continued loading of these structures can result in loss of the articular surface of
the condyle and fossa. The end result of this breakdown is osteoarthritis or degener-
ative joint disease (Fig. 3).
112 Okeson & de Leeuw

Fig. 3. The various states of internal derangement of the TMJ. (A) Normal joint. (B) Slight
disc displacement. (C) Disc displacement. (D) Impingement of the retrodiscal tissues. (E) Ret-
rodiscitis. (F) Osteoarthritis. (Adapted from Okeson JP. Management of temporomandibular
disorder and occlusion. 6th edition. St Louis (MO): CV Mosby; 2008. p. 197; with permission.)

Management considerations
As previously mentioned, a detailed description of the management of each of the
conditions is not the goal of this article and, therefore, other sources should be con-
sulted.3 However, because some simple behavior modifications may reduce the
loading of the joints, a few first-tier management options are described in this section.
Because comparative studies have shown that conservative therapies provide similar
results to the more aggressive ones, the general rule should always be to provide the
most conservative therapy first.
The principle concept for managing most intracapsular disorders is to reduce loading
of the joint structures so that remodeling and adaptation of the involved structures can
take place.17 It is important to note that for adaptation to take place and for normal func-
tion to return, it is not necessary to restore the disc position. The patient needs to know
that, if loading can be controlled, intracapsular disorders are often self limiting. Teaching
the patient to reduce loading by simple approaches such as a softer diet with slower
chewing can be very helpful. The patient should be instructed to avoid nonfunctional
tooth contacts, such as clenching the teeth, chewing gum, and other oral parafunctional
activity such as biting the fingernails or a pencil. If nighttime bruxism is suspected,
a stabilization appliance may be considered for sleep-related bruxism. In cases of a pain-
ful disc displacement with reduction, an anterior positioning appliance may be useful,
but care should be taken to use this appliance only during sleep, as longer use such
as during the day and night may result in malocclusion. Clock-regulated NSAIDs may
 Temporomandibular Disorders 113

also be helpful. Only after these types of therapies fail to control the patient’s pain should
more aggressive therapies be considered (eg, arthrocentesis or arthroscopy).

OTHER COMMON OROFACIAL PAIN DISORDERS

There are many conditions that manifest painful symptoms in the orofacial structures.
In fact, there are many textbooks that have been devoted solely to these condi-
tions.19,20 However, it is not the goal of this article to elaborate on all orofacial pain
conditions. The reader merely needs to appreciate that the scope of pain in the oro-
facial structures is multifaceted and complex. This article highlights a few of the
more common types of orofacial pain disorders that should be recognized by the clini-
cian so that patients may receive the most appropriate care. Many of these conditions
fall outside the normal realm of the dental practice and, therefore, should be referred to
other more appropriate health care providers. This article discusses four common oro-
facial pain conditions. The first two conditions are neuropathic pain conditions. Neuro-
pathic pain is a painful condition that has its origin within the neural tissue itself, either
peripherally or centrally. With neuropathic pain there is nothing wrong with the somatic
tissues; instead, the problem lies in how the nervous system is transmitting informa-
tion to the sensory cortex. Neuropathic pain is divided into episodic neuropathic
pain and continuous neuropathic pain disorders. The next two are migraine and
tension-type headache. These conditions are considered primary headaches by the
International Headache Society.21

Episodic Neuropathic Pains

Definition
As described earlier, pains that arise from abnormalities in the neural structures are
called “neuropathic pains.” Episodic neuropathic pains are characterized by a quick
off-and-on pattern of pain.

Clinical features
Episodic neuropathic pains are characterized by periods of very brief, but intense,
electrical shock-like pain followed by total remission. Usually, the individual is able
to localize the site of pain quite well. The site, however, does not identify the correct
source, because many are projected heterotopic pains. The term paroxysmal
neuralgia has been used to describe this electrical shock-like pain. The most common
is trigeminal neuralgia. Trigeminal neuralgia is characterized by a bright, stimulating,
electric shock-like-quality pain that radiates into one of the three branches of the
trigeminal nerve. The maxillary branch is affected most often, followed by the mandib-
ular branch. The ophthalmic branch is affected the least often. The pain is extremely
intense, usually lasting only a few seconds. On occasion it may last minutes, but this is
rare. The pain is typically brought on by innocuous stimuli such as touching the face,
shaving, or brushing the teeth. Between episodes the individual is usually pain free;
however, if the episodes are frequent, there may be a lingering, dull aching pain.22
Other neuralgias are glossopharyngeal neuralgia, geniculate neuralgia, superior laryn-
geal neuralgia, and nervus intermedius neuralgia.23

Etiologic considerations
The most common cause of trigeminal neuralgia is thought to be related to a demyeli-
nization of the nerve root as it exits the pons before reaching the foramen.24 This
demyelinization may be secondary to pressure applied to the nerve by either a vessel
in the brain25 or an intracranial tumor.26 Systemic demyelinization disorders such as
multiple sclerosis may also lead to symptoms indicative of trigeminal neuralgia.27
114 Okeson & de Leeuw

However, in the majority of cases, none such factors can be identified, which renders
the cause unknown.

Management considerations
Management of trigeminal neuralgia begins initially with medications that attempt to stabi-
lize the nerve membranes. The most effective medications are typically anticonvulsive
medications such as carbamazepine and oxcarbazepine, even though these medications
may have serious side effects.28–30 Medications with less evidence of effectiveness but
with a better side-effect profile include gabapentin31 or pregabalin.32 If medications do
not adequately resolve the pain, there are several surgical options varying from peripheral
procedures such as rhizotomy to central procedures, including microvascular decom-
pression surgeries and gamma knife procedures that may be considered.1

Continuous Neuropathic Pains

Definition
Some neuropathic pains may have fluctuating intensities but never go away. These
disorders are called continuous neuropathic pains and are currently some of the
most difficult orofacial pain conditions to successfully manage.

Clinical features
Continuous neuropathic pains are characterized by a dull, yet burning, pain. The pain
is ongoing and unremitting, yet the intensity can show patterns of fluctuation. The pain
is often accompanied by other neurologic signs (ie, anesthesia, paresthesia, hypoes-
thesia, hyperesthesia). Although the pain is present in a particular location, there is no
evidence of any tissue changes or disease. When this pain is felt in the region of the
teeth it can be a difficult challenge for the dentist. The pain may have the same clinical
characteristics of a true toothache, which makes the correct diagnosis challenging for
the clinician. However, helpful hints to consider are the duration of the pain and the
fact that stimulation of the site of neuropathic pain (ie, with hot or cold) does not typi-
cally influence the intensity of the pain.33

Etiologic considerations
The cause of continuous neuropathic pain is not well understood. Certainly, trauma to
a peripheral nerve can result in deafferentation (ie, an ongoing pain condition).34
However, some continuous neuropathic pains seem to spontaneously appear without
any obvious cause. It is believed that the central nervous system can change (neuro-
plasticity) resulting in the processing of information that is not appropriate for the
peripheral stimulus (central sensitization).

Management considerations
Management of continuous neuropathic pains is very difficult. Research is only begin-
ning to help us understand the central mechanisms that seem to contribute to this
painful condition. Medical management is the first line of treatment; however, the
medications that are presently available do not consistently help all patients. At
best, we can reduce pain and improve quality of life, but total elimination of this
type of pain is very difficult. Sometimes the tricyclic antidepressants35 such as amitrip-
tyline or desipramine can be helpful. The anticonvulsive medications such as gaba-
pentin or pregabalin may also be helpful.31,32,36 Often a trial of some of these
medications and others may be needed to determine the most effective treatment.
It is important to remember that neuropathic pains typically do not respond to NSAIDs
or opioids. A complete list of management options for continuous neuropathic pain
can be found elsewhere.
 Temporomandibular Disorders 115

Migraine
Definition
Migraine is a common, intense and debilitating headache. It is what the general public
refers to whenever someone has a “really bad headache.” It is a primary headache
with central etiologies. The International Headache Society has two major designa-
tions for migraine: migraine with aura and migraine without aura.37
Clinical features
Migraine is characterized by throbbing, moderate-to-severe, often debilitating pain.
Sixty percent of the time the headache is unilateral and often reported in the temple
or behind the eye. Migraine can be felt in the maxillary arch, thus referred to as “mid-
face migraine.” This can be a diagnostic problem for the dental clinician because the
pain can be felt in or around the teeth. The patient will often report nausea, photo-
phobia, phonophobia, and osmophobia, and will seek a dark, quiet room. The pain
is aggravated by routine physical activity and sometimes even simple head move-
ments. The pain episodes may occur at any time of the day or night but most
frequently occur on arising in the morning. The pain episode commonly lasts 4 to 72
hours in adults and 2 to 4 hours in children.38 Scalp tenderness occurs in two-thirds
of the patients during or after the headache.
Some migraine patients report a complex of focal neurologic symptoms that imme-
diately precedes the headache.39 This is called the “aura” and usually develops in 5 to
20 minutes and lasts less than 1 hour. When present, the aura is commonly character-
ized by visual, sensory, or motor phenomena, and may even include language and
brainstem disturbances. The visual symptoms are the most common phenomena
associated with aura. Visual symptoms can be characterized by sensations of flashes
of light before the eyes (photopsia), the partial loss of sight (scotoma), or a zigzag,
flashing colored phenomenon that migrates across the visual field (teichopsia).
Sensory symptoms such as paresthesia40 can occur. Motor effects may present as
focal fatigue or difficulty with speech.
Etiologic considerations
Migraine affects approximately 12% of the population, with about 18% females and
about 6% males being affected.41 Migraine most often appears in the first 3 decades
of life.
Studies suggest that migraine patients have a genetic susceptibility to this pain
condition, with 50% to 60% of migraine patients having parents that also experience
migraines.42 Migraine is considered a neurovascular phenomenon because both
neuralgic and vascular structures are involved in the pathophysiology. This system
of neural innervation of the intracranial vessels is called the trigeminovascular system.
Present evidence suggests that there is a neurologic trigger in the brainstem that initi-
ates a cascade of events that result in neurogenic inflammation of the cranial vessels
producing the headache.43
Management considerations
The management of migraine with or without aura involves patient education and
pharmacologic approaches. Patients who experience migraine headaches need to
understand basic information about their pain condition. They need to know that
even though the pain is very severe, it is still benign. An important aspect of education
is having the patient identify any triggering factors that initiate the migraine attack.
Triggers may be initiated by exposures to certain foods, alcohol, odors, stress, or
even changes in eating or sleeping patterns. The patient should be asked to maintain
a pain diary which helps identify factors that are associated with the initiation of the
116 Okeson & de Leeuw

headache. Once these factors are identified, efforts are made to avoid them so as to
reduce the number of migraine attacks.
Pharmacologic management of migraine can be divided into two types: medica-
tions that are used to abort a migraine at its start and medications that are used
to prevent migraine attacks. The choice of which management strategy to use is
determined by the frequency of the migraine attacks. As a general rule, migraine
attacks that are infrequent are managed with abortive medications so that treat-
ment is immediately initiated during the onset of the attack. When migraine
attacks occur so often that they significantly interfere with the patient’s daily activ-
ities, preventive medications should be considered.44 If abortive medications are
used 2 days per week or more, the patient may develop rebound headache or
medication-overuse headache.
A class of medications that has been proven helpful in aborting a migraine is the trip-
tans, of which there are many.44 These drugs seem to stop the neurogenic inflamma-
tion in the meningeal (dural) vasculature45 and they may also act within the brain.
Frequent migraines are best managed by prescribing daily medication so as to
prevent them from occurring. Beta-adrenergic agents (beta blockers) such as
propranolol or metoprolol46 or calcium channel blockers such as nifedipine or verap-
amil47 have proven effective. In addition, the tricyclic antidepressants have shown to
be useful—especially amitriptyline.44,48 Finally, anticonvulsants such as topiramate
and divalproex sodium also have proven to be efficacious in the prevention of
migraines.49
Dentists do not normally prescribe such medications unless they have advanced
training in orofacial pain, oral medicine, or oral surgery because many of the drugs
have significant side effects, especially on the cardiovascular system (eg, propranolol,
sumatriptan). Although most are quite safe in a healthy patient, the medically compro-
mised patient or chronic pain patient who uses other medications may experience
significant problems that will need proper attention by appropriate health care
professionals.
Tension-type Headache
Definition
Tension-type headache is a primary headache felt as a bilateral dull, aching pain usually
felt in the shape of a tight band around the head. It is estimated that as many as 74% of
the general population experience this type of headache at least once a year.50
Clinical features
Tension-type headache is the most common headache reported in the general pop-
ulation. The headache is described as a dull, nonpulsatile tightness, or pressure felt
in the occipital, parietal, temporal, and frontal regions. In 90% of the cases, the pain
is felt bilaterally.50 Some will describe the feeling of a tight “headband” compressing
their head as if they were wearing a tight cap. Most tension-type headaches are of mild
or moderate intensity, rarely becoming debilitating as with migraine. Most tension-
type headaches are episodic, lasting an average of 12 hours, although the duration
can vary greatly (30 minutes to 72 hours).51 Accompanying symptoms may consist
of either photophobia or phonophobia but not both. Nausea is not associated with
tension-type headache.52
Etiologic considerations
Although tension-type headache is the most common headache experienced by
humans, its pathophysiology remains unclear. Part of the problem may be that
tension-type headache likely has a central etiologic mechanism, especially involving
 Temporomandibular Disorders 117

the limbic structures. Emotional stress, anxiety, and depression seem to present
causal relationships with tension-type headaches.53,54 However, there are many other
disorders that result in headache that present with the same clinical characteristics of
tension-type headache. For example, trigger points associated with myofascial pain
(discussed previously) result in a headache at the referred site that is often clinically
described by the patient as a tension-type headache. This type of headache is
secondary to the myofascial condition and, therefore, should not be classified as
a tension-type headache. Similarly, patients with sleep bruxism may awake with head-
ache as a secondary symptom. Also morning headache in the temporal area is
frequent associated with sleep respiratory disorders related to snoring or sleep
apnea.55,56 The headache should always be classified to the primary disorder, which
will assist in selecting the proper treatment.
Management considerations
Like many pain disorders, management of tension-type headache begins with patient
education. The sufferer needs to identify those factors that aggravate the condition as
well as those that help relieve it. It is often helpful to have the patient maintain a head-
ache diary so that factors that are not commonly considered be recognized. The
patient should be encouraged to decrease intake of caffeine (coffee, tea, soft drinks)
and alcohol, as well as any medications that have been chronically used for the head-
ache (rebound headache). The patient should be informed that eliminating these
substances may at first increase the frequency and intensity of the headaches. After
1 to 2 weeks, the withdrawal effects should subside.
Since emotional stress often plays an important role in tension-type headache, the
patient should be assessed for any significant stressors and, if identified, corrective
behaviors or avoidance should be encouraged. Stress management skills can be
important therapies with tension-type headache. Relaxation training and biofeedback
techniques53,54 can also be very helpful. All these are frequently performed by
a psychologist trained in cognitive-behavioral therapy. If a major depression disorder
or anxiety disorder is present, these conditions need to be managed by the proper
health care provider.
As with migraines, depending on the frequency of the headache, tension-type head-
aches are treated either with abortive or preventive medications. However, there are to
date no evidence-based guidelines indicating which medications are most effective.
To abort infrequent tension-type headaches, judicious use of mild analgesics (eg,
aspirin, ibuprofen) may be needed, but the patient should be aware of the potential
complications. NSAIDs are often helpful, especially if the patient has not been using
them previously. If one NSAID is not effective, another should be tried. To prevent
frequent tension-type headaches low dosages of a tricyclic antidepressant such as
nortriptyline and amitriptyline can be helpful. They are best taken before bed time
because of their sedative effects.
When the tension-type headache symptoms are secondary to another disorder,
therapy needs to be extended to that disorder. For example, when the headache is
associated with a masticatory muscle disorder, the muscle disorder needs to be
managed.3 Headache upon awaking may be related to nocturnal bruxism or sleep
breathing disorders (apnea-hypopnea syndrome) and several approaches can be
used to address this.

SUMMARY

There are many types of pain conditions that produce orofacial pain. The most
common are dental and periodontal pains, which are highlighted elsewhere in this
118 Okeson & de Leeuw

issue. Some of the other common pain disorders are musculoskeletal, which in the
orofacial structures are called TMD. These disorders need to be identified by the
dentist. In most cases they can be managed by relatively simple strategies. There
are still many other pain disorders of the head and neck that are unrelated to the dental
structures. The dentist should be able to differentiate these and refer the patient to the
appropriate health care provider for appropriate care.

REFERENCES

1. De Leeuw R. Orofacial pain: guidelines for classification, assessment, and

management. 4th edition. Chicago: Quintessence Publ. Co.; 2008.
2. Griffiths RH. Report of the President’s Conference on Examination, Diagnosis and
Management or Temporomandibular Disorders. J Am Dent Assoc 1983;106:75–7.
3. Okeson JP. Management of temporomandibular disorders and occlusion. 6th
edition. St Louis (MO): The CV Mosby Company; 2008.
4. Simons DG, Travell JG, Simons LS, et al. Pain and dysfunction: a trigger point
manual. 2nd edition. Baltimore (MD): Williams & Wilkins; 1999.
5. Mense S. The pathogenesis of muscle pain. Curr Pain Headache Rep 2003;7(6):
419–25.
6. Glaros AG, Burton E. Parafunctional clenching, pain, and effort in temporoman-
dibular disorders. J Behav Med 2004;27(1):91–100.
7. Carlson CR, Okeson JP, Falace DA, et al. Comparison of psychologic and phys-
iologic functioning between patients with masticatory muscle pain and matched
controls. J Orofac Pain 1993;7:15–22.
8. Lund JP, Widmer CG. An evaluation of the use of surface electromyography in the
diagnosis, documentation, and treatment of dental patients. J Craniomandib Dis-
ord 1988;3:125–37.
9. Klasser GD, Okeson JP. The clinical usefulness of surface electromyography in
the diagnosis and treatment of temporomandibular disorders. J Am Dent Assoc
2006;137(6):763–71.
10. Okeson JP. Bell’s orofacial pains. 6th edition. Chicago: Quintessence Publishing
Co Inc; 2005. Chapter 595–104.
11. Carlson C, Bertrand P, Ehrlich A, et al. Physical self-regulation training for the
management of temporomandibular disorders. J Orofac Pain 2001;15:47–55.
12. Bell WE. Temporomandibular joint disease. Dallas (TX): Egan Company; 1960.
13. Nitzan DW. ’Friction and adhesive forces’–possible underlying causes for tempo-
romandibular joint internal derangement. Cells Tissues Organs 2003;174(1–2):
6–16.
14. Yun PY, Kim YK. The role of facial trauma as a possible etiologic factor in tempo-
romandibular joint disorder. J Oral Maxillofac Surg 2005;63(11):1576–83.
15. Zhang ZK, Ma XC, Gao S, et al. Studies on contributing factors in temporoman-
dibular disorders. Chin J Dent Res 1999;2(3–4):7–20.
16. Grushka M, Ching VW, Epstein JB, et al. Radiographic and clinical features of
temporomandibular dysfunction in patients following indirect trauma: a retrospec-
tive study. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2007;104(6):
772–80.
17. Brandt KD, Dieppe P, Radin E. Etiopathogenesis of osteoarthritis. Med Clin North
Am 2009;93(1):1–24, xv.
18. Milam SB, Zardeneta G, Schmitz JP. Oxidative stress and degenerative temporo-
mandibular joint disease: a proposed hypothesis. J Oral Maxillofac Surg 1998;
56(2):214–23.
 Temporomandibular Disorders 119

19. Olesen JGP, Ramandon N, Tfelt-Hansen P, et al. The headaches. 3rd edition. Phil-
adelphia: Lippincott, Williams and Wilkins; 2006.
20. Dalessio DJ, Silberstein SD. Wolff’s headache and other head pain. 6th edition.
New York: Oxford University Press; 1993.
21. Olesen J. The international classification for headache disorders. Cephalalgia
2004;24(Suppl 1):1–160.
22. McArdle MJ. Atypical facial neuralgia. In: Hassler R, Walker AE, editors. Trigem-
inal neuralgia. Stuttgart (Germany): Georg Thieme Verlag; 1970. p. 35–42.
23. Okeson JP. Bell’s orofacial pains. 5th edition. Chicago: Quintessence Publishing
Co, Inc; 1995. Chapter 17. p.403–55.
24. Devor M, Amir R, Rappaport ZH. Pathophysiology of trigeminal neuralgia: the
ignition hypothesis. Clin J Pain 2002;18(1):4–13.
25. Love S, Coakham HB. Trigeminal neuralgia: pathology and pathogenesis. Brain
2001;124(Pt 12):2347–60.
26. Celik SE, Kocaeli H, Cordan T, et al. Trigeminal neuralgia due to cerebellopontine
angle lipoma. Case illustration. J Neurosurg 2000;92(5):889.
27. Fiske J, Griffiths J, Thompson S. Multiple sclerosis and oral care. Dent Update
2002;29(6):273–83.
28. Wiffen PJ, McQuay HJ, Moore RA. Carbamazepine for acute and chronic pain.
Cochrane Database Syst Rev 2005;3:CD005451.
29. Gomez-Arguelles JM, Dorado R, Sepulveda JM, et al. Oxcarbazepine monother-
apy in carbamazepine-unresponsive trigeminal neuralgia. J Clin Neurosci 2008;
15(5):516–9.
30. Nasreddine W, Beydoun A. Oxcarbazepine in neuropathic pain. Expert Opin In-
vestig Drugs 2007;16(10):1615–25.
31. Gilron I, Bailey JM, Tu D, et al. Nortriptyline and gabapentin, alone and in combi-
nation for neuropathic pain: a double-blind, randomised controlled crossover
trial. Lancet 2009;374(9697):1252–61.
32. van Seventer R, Feister HA, Young JP Jr, et al. Efficacy and tolerability of twice-
daily pregabalin for treating pain and related sleep interference in
postherpetic neuralgia: a 13-week, randomized trial. Curr Med Res Opin 2006;
22(2):375–84.
33. Graff-Radford SB, Solberg WK. Atypical odontalgia. J Craniomandib Disord
1992;6(4):260–5.
34. Fields HL, Rowbotham M, Baron R. Postherpetic neuralgia: irritable nociceptors
and deafferentation. Neurobiol Dis 1998;5(4):209–27.
35. Haanpaa ML, Gourlay GK, Kent JL, et al. Treatment considerations for patients
with neuropathic pain and other medical comorbidities. Mayo Clin Proc 2010;
85(3 Suppl):S15–25.
36. Jensen TS, Madsen CS, Finnerup NB. Pharmacology and treatment of neuro-
pathic pains. Curr Opin Neurol 2009;22(5):467–74.
37. Oleson J, Tfelt-Hansen P, Welch KM. The headaches. 2nd edition. Philadelphia:
Lippincott, Williams and Wilkins; 1999.
38. Lipton RB, Bigal ME, Steiner TJ, et al. Classification of primary headaches.
Neurology 2004;63(3):427–35.
39. Stewart WF, Shechter A, Lipton RB. Migraine heterogeneity. Disability, pain inten-
sity, and attack frequency and duration. Neurology 1994;44(6 Suppl 4):S24–39.
40. Russell MB, Olesen J. A nosographic analysis of the migraine aura in a general
population. Brain 1996;119(Pt 2):355–61.
41. Lipton RB, Bigal ME, Diamond M, et al. Migraine prevalence, disease burden,
and the need for preventive therapy. Neurology 2007;68(5):343–9.
120 Okeson & de Leeuw

42. Walters WE, Silberstein SD, Dalessio DJ. Inheritance and epidemiology of head-
ache. In: Dalessio DJ, Silberstein SD, editors. Wolff’s headache and other head
pain. 6th edition. New York: Oxford University Press; 1993. p. 42–58.
43. Lambert GA, Zagami AS. The mode of action of migraine triggers: a hypothesis.
Headache 2009;49(2):253–75.
44. Silberstein SD. Practice parameter: evidence-based guidelines for migraine
headache (an evidence-based review): report of the Quality Standards Subcom-
mittee of the American Academy of Neurology. Neurology 2000;55(6):754–62.
45. Williamson DJ, Hargreaves RJ. Neurogenic inflammation in the context of
migraine. Microsc Res Tech 2001;53(3):167–78.
46. Diener H. Pharmacological approaches to migraine. J Neural Transm Suppl 2003;
64:35–63.
47. Adelman JU, Adelman RD. Current options for the prevention and treatment of
migraine. Clin Ther 2001;23(6):772–88 [discussion: 71].
48. Bendtsen L, Jensen R. Amitriptyline reduces myofascial tenderness in patients
with chronic tension-type headache. Cephalalgia 2000;20(6):603–10.
49. Mulleners WM, Chronicle EP. Anticonvulsants in migraine prophylaxis: a Cochrane
review. Cephalalgia 2008;28(6):585–97.
50. Rasmussen BK, Jensen R, Olesen J. A population-based analysis of the criteria
of the International Headache Society. Cephalalgia 1991;11:129–34.
51. Iversen HK, Langemark M, Andersson PG, et al. Clinical characteristics of
migraine and tension-type headache in relation to new and old diagnostic criteria.
Headache 1990;30:514–9.
52. Olesen J, Lipton RB. Headache classification update 2004. Curr Opin Neurol
2004;17(3):275–82.
53. Holte KA, Vasseljen O, Westgaard RH. Exploring perceived tension as a response
to psychosocial work stress. Scand J Work Environ Health 2003;29(2):124–33.
54. Bertolotti G, Vidotto G, Sanavio E, et al. Psychological and emotional aspects and
pain. Neurol Sci 2003;24(Suppl 2):S71–5.
55. Bailey DR. Tension headache and bruxism in the sleep disordered patient. Cranio
1990;8(2):174–82.
56. Ozge A, Ozge C, Kaleagasi H, et al. Headache in patients with chronic obstruc-
tive pulmonary disease: effects of chronic hypoxaemia. J Headache Pain 2006;
7(1):37–43.